The mammalian intestine is colonized by an estimated 100 trillion bacteria, which have co-evolved with the host in a symbiotic relationship. This collection of microbial populations in the host is referred to as the microbiota. The microbiota can efficiently protect the intestine against colonization by exogenous pathogens and potentially harmful indigenous microorganisms (pathobionts). Mucosal immune responses to normal intestinal bacteria are also important for development and physiology of the host. Breakdown in immunological tolerance to microbiota lead to inappropriate local and systemic immune responses to intestinal bacterial communities that may contribute to multiple disease states such as inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). The increased prevalence of these chronic conditions has been suggested to be influenced by factors including bacterial infections, antibiotic exposure, as well as dietary factors, stress and degree of hygiene.
Alteration in the balance of the intestinal microbiota results in disrupted intestinal homeostasis, which increases the risk of pathogen infection and the overgrowth of pathobionts, particularly in immunocompromised hosts. Pathobionts are typically colitogenic in that they can trigger intestinal inflammation. Pseudomembranous colitis which results in severe diarrhea, fever and abdominal pain, is caused by overgrowth of Clostridium difficile (CD), a Gram-positive anaerobic bacterium, following long-term treatment with broad-spectrum antibiotics.
Long-term hospitalization, antibiotic treatment, immune deficiency, cancerous diseases, chemotherapy, and steroid treatment are the main causes of nosocomial diarrhea infections triggered usually by CD but also other enteric bacterial pathogens such as Salmonella, Shigella, Camphylobacter, and Yersinia. 
CD has become one of the most serious causes of antibiotic-associated diarrhea. Conventional treatment includes vancomycin or metronidazole for ten days. However, recurrence (occurs in 10 to 25% of cases) is getting increasingly common and represent the greatest challenge associated with CD infections (CDI).
Increasing rates of CDI have been reported in Canada and the United States, with a larger proportion of severe and recurrent cases than previously reported. In US, the rates of hospital discharges with CDI listed as any diagnosis increased from 3.82 per 1000 discharges in 2000 to 8.75 per 1000 discharges in 2008; increases were especially prominent among those ≥65 years of age. Preliminary data indicate that the number of death certificates with enterocolitis due to CDI increased from 793 in 1999 to 7483 in 2008 in US. The rate of pediatric CDI-related hospitalizations also increased between 1997 and 2006, from 0.724 to 1.28 per 1000 hospitalizations. The highest incidence was reported in children 1-4 years of age. The raised incidence and virulence of CDI have coincided with the spread of the hypervirulent CD referred to as NAP1/027, also known as CD BUNAP1/027 (a restriction endonuclease analysis group BI, pulse-field gel electrophoresis type NAP1, and polymerase chain reaction ribotype 027). NAP1/027 strain produces a binary toxin and up to 16-fold more toxins than most other hospital outbreak associated strains. Subsequently, epidemics of CDI caused by CD NAP1/027 have been recognized in hospitals in European countries, e.g. the United Kingdom, the Netherlands, Belgium, Austria, and Sweden. The major changes in the epidemiology of CDI during recent years, with increases in incidence and severity of disease have made it a global public health challenge.
The only products used to treat CDI are antibiotics, such as metronidazole, vancomycin, and the recently approved Dificid. Although their high clinical cure rates, 15-30% of patients still experience a recurrence, with each recurrence increasing the risk of further infections. Both the appropriate and the inappropriate use of antibiotics are also associated with the rise in resistance to antibiotics, the emergence of vancomycin resistant new biotypes of Clostridium difficile, and the increasing incidence of chronic inflammatory conditions.
The rates of severe cases of CDI have increased during the recent years and the hypervirulent CD NAP1/027 has been associated with recent outbreaks throughout the world. European Centre for Disease Prevention and Control (ECDC) found (in 2011) that the prevalence of CD NAP1/027 was 5% in the 34 European countries. Large outbreaks of severe, often fatal, colitis have also been reported in North America and Europe. Such an infection may, as a last option when no other treatment has been effective, be treated by the transplantation of feces from a healthy individual. Such transplantation, in addition to the possible psychological discomfort, may also pose the risk of transplanting potentially harmful microorganisms from the donor. Thus, although fecal microbiota transplant has demonstrated some promising results for treating CDI, physicians are concerned about potential infection risks and long-term safety. Recent reports on an obesity onset followed after a fecal transplantation indicate risks and long-term safety issues. In addition, the cumbersome procedures associated with the technology limit its routine use. There are no standard protocols and procedures regarding donor screening/selection, preparation of fecal materials, sanitation issues, recipient preparation, and route of administration.
Thus, there is a need for more effective therapeutic treatment options as well as preventative treatments for CDI.
An altered composition of microbiota interferes with normal intestinal functions at diverse levels. In addition to triggering the immune system and proinflammatory cytokines, it may also induce release of microbial metabolites, activation of hypothalamic-pituitaryadrenal (HPA) axis with increase of cortisol, leading to alterations of intestinal motility and sensation, disruption of intestinal barrier and impaired production of neurotransmitters with an increased response to stressful events. These complications may cause the IBS which is a chronic functional disorder of the gastrointestinal system and of the most common causes of illness and workplace absenteeism. No cure is available and IBS patients have to rely on treatments to relive symptoms such pain, diarrhea and constipation, associated with side effects. The cause of IBS is unknown but there is increasing evidence showing changes in the composition of luminal and mucosal microbiota among IBS patients compared to healthy individuals. Examples of these modifications are a decreased amount of lactobacilli and bifidobacteria along with an increased amount of Clostridium in IBS patients. Investigations of gut microbiota of children diagnosed with IBS also indicates a dysbiosis mainly dominated by Clostridium. 
Therapeutic interventions using lactobacilli are therefore attractive in IBS. A number of studies have concluded that lactobacilli, in general, benefit patients with IBS but it has been difficult to define relative benefits of different bacterial strains. Weak effects and mixed results are primarily due to lack of proper bacterial strain selection and the often poor quality of the studies.